ライフサイエンスコーパス: CML

1 CML and sRAGE were measured by ELISA, and the CML/sRAGE

2 CML cells from chronic phase CML patients as well as the

3 CML concentrations ranged from 2 to 210 ug/g protein in

4 CML concentrations were higher in individuals with highe

5 CML patients with and without diarrhoea on the SPIRIT2 t

6 CML progenitors demonstrated enhanced sensitivity to Wnt

7 CML therapy based on tyrosine kinase inhibitors (TKIs) i

8 s, including primary cells explanted from 12 CML patients.

9 None of the patients experienced a CML progression.

10 ort new data on the biological function of a CML-interacting partner, PRR2 (PSEUDO-RESPONSE REGULATOR

11 gonist, conferred similar protection against CML.

12 d selective PORCN inhibitor, WNT974, against CML stem and progenitor cells.

13 discovery in patients almost 2 decades ago, CML LSCs have become a well-recognized exemplar of the c

14 However, in stratified analyses, CML was positively associated with SAF after excluding b

15 ngerol also decreased the levels of AGEs and CML levels, via Nrf2 pathway, enhancing GSH/GSSG ratio,

16 This increased risk of AML and CML after RAI treatment was seen even in low-risk and in

17 n increased early risk of developing AML and CML but no other hematologic malignancies.

18 Furthermore, LSCs from both AML and CML can be refractory to standard-of-care therapies and

19 CaM and CML regulate a wide range of target proteins and cellula

20 dy suppressed human CML colony formation and CML repopulation in vivo.

21 novo in samples from healthy volunteers and CML patients.

22 rs therefore of primary importance to aim at CML eradication.

23 cells and increased sCD62L plasma levels at CML diagnosis on molecular response to tyrosine kinase i

24 cells and, vice versa, low sCD62L levels at CML diagnosis were linked to superior molecular response

25 4+ T cell-mediated GVL against CP-CML and BC-CML required intact leukemia MHCII; however, stem cells

26 Mouse AML and BC-CML stem cells were MHCI+ without IFN-gamma stimulation,

27 leukemia (CP-CML), but blast crisis CML (BC-CML) and acute myeloid leukemias (AML) are GVL resistant

28 udied GVL against mouse models of CP-CML, BC-CML, and AML generated by the transduction of mouse BM w

29 Here, we show that CP-CML, BC-CML, and AML stem cells upregulate MHCII in alloSCT reci

30 Importantly, IFN-gammaR-deficient BC-CML and AML were completely resistant to CD4- and CD8-me

31 IFN-gamma stimulation as a mechanism for BC-CML and AML GVL resistance, whereas independence from IF

32 e-deficient leukemias, we determined that BC-CML and AML MHC upregulation required IFN-gamma stimulat

33 Because CML is a model immune system-sensitive disease, we hypot

34 Because CML is such an ideal model, new methods are arising that

35 at CML cells express low levels of TNTs, but CML therapeutics increase TNT formation in designated ce

36 ine-driven JAK-mediated signals, provided by CML cells and/or the microenvironment, antagonize MHC-II

37 CaM/CMLs decode and relay information encrypted by the secon

38 ), including N(epsilon)-carboxymethyllysine (CML) formed between lysine and lactose.

39 reduction of N-epsilon-carboxymethyllysine (CML), secoiridoids were effective only in model systems

40 reactions revealed that exposure of CD34(+) CML cells to IFN-gamma or RUX significantly enhanced pro

41 ulation in CML lines and primary human CD34+ CML stem cells.

42 I review how changing CML practices can impact HAI rates and how the financial

43 hile one class of patients required complete CML eradication to achieve TFR, other patients were able

44 ntration of protein bound Amadori compounds, CML, CEL and dicarbonyls.

45 A series of 236 consecutive CML patients with failure (n = 124) or warning (n = 112)

46 chanisms that promote the survival of the CP CML LSCs and how they can be a source of new gene coding

47 own that CD4+ T cell-mediated GVL against CP-CML and BC-CML required intact leukemia MHCII; however,

48 hereas IFN-gammaR/IFNAR1 double-deficient CP-CML was fully GVL sensitive.

49 h chronic phase chronic myeloid leukemia (CP-CML) are treated with tyrosine kinase inhibitors (TKIs).

50 ronic phase chronic myelogenous leukemia (CP-CML), but blast crisis CML (BC-CML) and acute myeloid le

51 e, we studied GVL against mouse models of CP-CML, BC-CML, and AML generated by the transduction of mo

52 ereas independence from IFN-gamma renders CP-CML more GVL sensitive, even with a lower-level alloimmu

53 Here, we show that CP-CML, BC-CML, and AML stem cells upregulate MHCII in allo

54 n required IFN-gamma stimulation, whereas CP-CML MHC upregulation was independent of both the IFN-gam

55 nd prognostic impact of 598 patients with CP-CML treated on clinical trials with various TKIs.

56 logenous leukemia (CP-CML), but blast crisis CML (BC-CML) and acute myeloid leukemias (AML) are GVL r

57 not only is activated in human blast crisis CML and de novo acute myeloid leukaemia, but also predic

58 and impairs the propagation of blast crisis CML both in vitro and in vivo.

59 tion through BCAA production in blast crisis CML cells.

60 ng protein that is required for blast crisis CML.

61 nd survival in secondary organs, which curbs CML development, progression, and metastatic disseminati

62 and individuals with CKD: 1 SD higher daily CML intake was associated with a 0.03 (95% CI: 0.009, 0.

63 domly assigned patients with newly diagnosed CML in the chronic phase to receive either imatinib or i

64 Higher dietary CML intake was associated with higher SAF only among par

65 During CML development, abnormal clusters of colocalized MSCs a

66 ollowing treatment with the highly effective CML therapeutics tyrosine kinase inhibitors (TKIs) and i

67 f PTN has therapeutic potential to eradicate CML stem cells.

68 d to complete disease control and eradicated CML xenograft tumours without recurrence after the cessa

69 protein translation, selectively eradicates CML LSCs both in vitro and in a xenotransplantation mode

70 diarrhoea in ~10% of imatinib-treated female CML patients.

71 supports the implementation of ELISA in food CML/AGEs screening.

72 Mean +/- SD intake was 3.40 +/-0.89 mg/d for CML, 28.98 +/-7.87 mg/d for MGH1, and 3.11 +/-0.89 mg/d

73 CL6 expression was shown to be essential for CML stem cell survival and self-renewal during imatinib

74 ABL kinase inhibitor approved by the FDA for CML treatment.

75 an ordinary differential equation model for CML, which explicitly includes an antileukemic immunolog

76 l-autonomous PTN signaling was necessary for CML disease evolution.

77 mal residual disease and are responsible for CML relapse following discontinuation of treatment.

78 nd require cell-autonomous PTN signaling for CML pathogenesis in BCR/ABL+ mice.

79 ysates of cow whey proteins, were tested for CML levels using a commercially available ELISA kit.

80 hibitors could provide effective therapy for CML.

81 atological benign specimens and samples from CML patients in deep molecular remission delineated a pa

82 Additionally, the frontline CML treatment with second-generation TKIs produces deepe

83 Higher CML and sRAGE concentrations were also associated with h

84 rn immunoblotting techniques detected higher CML levels in whey proteins compared with casein.

85 ry protein intake was associated with higher CML and sRAGE concentrations in older adults; however, t

86 Human CML cells were also dependent on cell-autonomous PTN sig

87 d abrogated self-renewal in murine and human CML stem/progenitor cells.

88 In both human CML K562 cells and murine Ba/F3 cells expressing BCR-ABL

89 ficiently antagonized Wnt signaling in human CML CD34(+) cells, and in combination with the TKI nilot

90 colony or cluster-forming capacity of human CML stem cells in the absence or presence of IM, respect

91 etely blocked the cluster formation of human CML stem cells.

92 and in a xenotransplantation model of human CML.

93 ling, and anti-PTN antibody suppressed human CML colony formation and CML repopulation in vivo.

94 -cell responses against the newly identified CML-associated peptides in CML patient samples and their

95 In CML, the acquisition of the fusion tyrosine kinase BCR-A

96 In CML, the BCR-ABL1 fusion gene and its companion messenge

97 -molecule-induced degradation of BCR-ABL1 in CML provides an advantage over inhibition and provides i

98 promise for strengthening immune control in CML but requires the identification of CML-associated ta

99 transactivator (CIITA) are downregulated in CML compared with non-CML stem/progenitor cells in a BCR

100 nodrug could upregulate FRbeta expression in CML cancer cells and xenograft tumor model, facilitating

101 zed if IFNgamma modulates BCL6 expression in CML cells.

102 embers of the BCL2 and BIRC gene families in CML cells, including the long isoform of MCL1, which pro

103 ell-extrinsic disruption of hematopoiesis in CML associated with clinical outcome.

104 , direct upregulation of BCL6 by IFNgamma in CML cells.

105 ed in an upregulation of CIITA and MHC-II in CML stem/progenitor cells; however, the extent of IFN-ga

106 n on CD4(+)/CD8(+) T cells were increased in CML patients at diagnosis.

107 iated with a 13.3 +/- 3.0 ng/ml increment in CML and a 22.1 +/- 6.0 pg/ml increment in sRAGE (P < 0.0

108 s and differences that exist between LSCs in CML and AML and examine the therapeutic strategies that

109 newly identified CML-associated peptides in CML patient samples and their ability to induce multifun

110 eneity within the putative LSC population in CML at diagnosis and demonstrate differences in response

111 at interferon gamma (IFNgamma) production in CML patients might have a central role in the response t

112 d regulation of survival and self-renewal in CML cells with leukemic-initiating capacity that can be

113 effector and suppressor immune responses in CML patients at diagnosis (n = 21), on TKI (imatinib, ni

114 hods are arising that should make testing in CML faster, more reliable, and reach a greater sensitivi

115 um supplementation as an adjuvant therapy in CML.

116 Here, we have investigated TNTs in CML cells and following treatment with the highly effect

117 ment induced remarkable BCL6 upregulation in CML lines and primary human CD34+ CML stem cells.

118 ner, we searched for such vulnerabilities in CML LSCs.

119 The NEXT-in-CML study provides for the first time robust demonstrati

120 ed a prospective, multicenter study (NEXT-in-CML) to assess the frequency and clinical relevance of l

121 ed the maintenance of BCR-ABL1(p210)-induced CML by impairing survival and self-renewal in BCR-ABL1+

122 FZD4 knockdown inhibited CML progenitor growth.

123 y and increased CyPG levels, which inhibited CML progression.

124 bers of CML stem cells capable of initiating CML in vivo.

125 e over inhibition and provides insights into CML stem cell biology.

126 ces in the clinical microbiology laboratory (CML) provide more-precise and -sensitive tests, altering

127 at milk formulas contained 7 to 12-fold less CML than cow milk formulas.

128 m cells (LSCs) in chronic myeloid leukaemia (CML) and acute myeloid leukaemia (AML) have been advance

129 ally required for chronic myeloid leukaemia (CML) in humans and in mouse models of CML.

130 Chronic myeloid leukaemia (CML) is driven by the activity of the BCR-ABL1 fusion on

131 ent of choice for chronic myeloid leukaemia (CML), can cause lower gastrointestinal (GI) toxicity whi

132 inases in K-562 chronic myelocytic leukemia (CML) cells elicited by treatment with imatinib, an ABL k

133 e treatment of chronic myelogenous leukemia (CML) largely depends on the eradication of CML leukemic

134 ual disease in chronic myelogenous leukemia (CML) may be relevant for long-term control or cure of CM

135 n to alleviate chronic myelogenous leukemia (CML) via the elimination of leukemia stem cells (LSCs) i

136 patients with chronic myelogenous leukemia (CML), but the persistence of CML stem cells hinders cure

137 rs (GISTs) and chronic myelogenous leukemia (CML).

138 primarily to treat chronic myeloid leukemia (CML) and gastrointestinal stromal tumors (GIST).

139 gnancies including chronic myeloid leukemia (CML) and myelodysplastic syndromes (MDS) either sensitiv

140 city in live human chronic myeloid leukemia (CML) cell lines.

141 positive (FRbeta+) chronic myeloid leukemia (CML) cells, resulting in more intracellular accumulation

142 ith an established chronic myeloid leukemia (CML) fusion gene (BCR-ABL1) assay down to 0.01% mutant a

143 (TKI) treatment of chronic myeloid leukemia (CML) has limited efficacy against leukemia stem cells (L

144 d for treatment of chronic myeloid leukemia (CML) in adults treated with tyrosine kinase inhibitors (

145 leukemia (AML) and chronic myeloid leukemia (CML) incidences remained constant prior to 2011 but have

146 Chronic myeloid leukemia (CML) is a chronic disease resulting in myeloid cell expa

147 Chronic myeloid leukemia (CML) is a hematopoietic stem cell (HSC)-driven neoplasia

148 Chronic myeloid leukemia (CML) is a stem cell disease of the bone marrow where mec

149 Chronic myeloid leukemia (CML) is caused by the acquisition of the tyrosine kinase

150 Chronic myeloid leukemia (CML) is currently treated with tyrosine kinase inhibitor

151 obstacle to curing chronic myeloid leukemia (CML) is the intrinsic resistance of CML stem cells (CMLS

152 Chronic myeloid leukemia (CML) is the model cancer, demonstrating the clinical ben

153 Patients with chronic myeloid leukemia (CML) often have comorbidities, at an incidence that migh

154 Chronic myeloid leukemia (CML) originates in a hematopoietic stem cell (HSC) trans

155 n in chronic phase chronic myeloid leukemia (CML) patients at diagnosis and following conventional ty

156 ecular response in chronic myeloid leukemia (CML) patients on tyrosine kinase inhibitor (TKI) therapy

157 In chronic myeloid leukemia (CML) patients, tyrosine kinase inhibitors (TKIs) may sel

158 hly upregulated as chronic myeloid leukemia (CML) progressed from the chronic phase to the blast cris

159 f highly quiescent chronic myeloid leukemia (CML) SCs that is enriched following therapy with tyrosin

160 in treatment-naive chronic myeloid leukemia (CML) stem/progenitor cells and identified that miR-185 l

161 s in patients with chronic myeloid leukemia (CML) suggest that the risk of molecular recurrence after

162 from patients with chronic myeloid leukemia (CML) throughout the disease course, revealing heterogene

163 ificantly affected chronic myeloid leukemia (CML) treatment, transforming the life expectancy of pati

164 n a mouse model of chronic myeloid leukemia (CML) triggers the release of LSCs from the BM into the c

165 d in patients with chronic myeloid leukemia (CML) who have had undetectable minimal residual disease

166 Treatment of chronic myeloid leukemia (CML) with imatinib mesylate and other second- and/or thi

167 Chronic myeloid leukemia (CML), caused by constitutively active BCR-ABL1 fusion ty

168 s in patients with chronic myeloid leukemia (CML), issues of drug resistance and residual leukemic st

169 ged the outcome of chronic myeloid leukemia (CML), turning a life-threatening disease into a chronic

170 gnancies including chronic myeloid leukemia (CML), where BCL6 expression was shown to be essential fo

171 iesis resembling a chronic myeloid leukemia (CML)-like disease manifesting in "lymphoid blast crisis.

172 a murine model of chronic myeloid leukemia (CML)-like myeloproliferative neoplasia by repressing an

173 ced mouse model of chronic myeloid leukemia (CML).

174 ancerous states in chronic myeloid leukemia (CML).

175 for patients with chronic myeloid leukemia (CML).

176 discontinuation in chronic myeloid leukemia (CML).

177 -free remission in chronic myeloid leukemia (CML).

178 2.82; P = .01) and chronic myeloid leukemia (CML; hazard ratio, 3.44; 95% CI, 1.87 to 6.36; P < .001)

179 n (CaM) and closely related calmodulin-like (CML) polypeptides are principal sensors of Ca(2+) signal

180 Calmodulin-like (CML) proteins are major EF-hand-containing, calcium (Ca(

181 ted by Calmodulin (CaM) and calmodulin-like (CML) proteins is critical to plant immunity.

182 as made from intact proteins contained lower CML compared to formulas using whey hydrolysates.

183 ibition of N(epsilon)-(carboxymethyl)lysine (CML) formation.

184 f AGEs and N(epsilon)-(carboxymethyl)lysine (CML) found to be predominantly higher in the diabetic po

185 rotein-bound Nepsilon-(carboxymethyl)lysine (CML), Nepsilon-(1-carboxyethyl)lysine (CEL), and pentosi

186 tions of the major AGE carboxymethyl-lysine (CML) and the soluble receptor for AGEs (sRAGE) in 2439 p

187 N(epsilon)-carboxymethyl-lysine (CML) is measured in food, but there is a controversy con

188 ts, intake of 3 dAGEs [carboxymethyl-lysine (CML), N-(5-hydro-5-methyl-4-imidazolon-2-yl)-ornithine (

189 Median CML concentrations were up to 3-fold greater in formulas

190 +)CD4(+)/CD8(+) T cells persisted in pre-MMR CML patients on TKI.

191 obtained by ELISA performed with monoclonal CML-antibody (beta=0.98, p<0.0001) whereas My Bio Source

192 esponsible for disease propagation, and most CML patients require continued TKI treatment to maintain

193 d significantly prolongs survival in a mouse CML model, with a negligible effect on HSCs.

194 Moreover, in a murine CML model, ACF decreased leukemia development and reduce

195 nd activity of LSCs in a pre-clinical murine CML model and a xenograft model of transplanted CML pati

196 ted significantly less-severe effects on non-CML hematopoietic cells in vitro and in vivo.

197 nificantly lower than when compared with non-CML CD34(+) cells.

198 ) are downregulated in CML compared with non-CML stem/progenitor cells in a BCR-ABL kinase-independen

199 Occurrence of AML but not CML in patients with WDTC was associated with shorter me

200 ays and HPLC-ESI-ITMS/MS for the analysis of CML in several food items.

201 ty to AML LSCs not observed in most cases of CML.

202 ell immunotherapy approach in the context of CML that is applicable for young patients and primary TK

203 sed by leukemic stem cells in the context of CML.

204 g TKI-free survival and even mediate cure of CML patients.

205 be relevant for long-term control or cure of CML.

206 Small differences of CML concentrations in food items prepared by different c

207 relation (0.853-0.990) with effectiveness of CML inhibition, except in the case of samples with FA.

208 (CML) largely depends on the eradication of CML leukemic stem cells (LSCs).

209 entially lead to the complete eradication of CML stem cells.

210 o assist in the detection and eradication of CML stem/progenitor cells.

211 Free forms of CML, CEL, and Ndelta-(5-hydro-5-methyl-4-imidazolon-2-yl

212 avine (ACF) decreased survival and growth of CML cells.

213 e disease course, revealing heterogeneity of CML-SCs, including the identification of a subgroup of C

214 ol in CML but requires the identification of CML-associated targets.

215 upplemented with PCs contained low levels of CML, this process may adversely affect bread flavor, red

216 lator of LSC survival, on the maintenance of CML stem cell potential.

217 aemia (CML) in humans and in mouse models of CML.

218 eletion substantially reduced the numbers of CML stem cells capable of initiating CML in vivo.

219 methods showed the same decreasing order of CML concentration: beef, bacon>chicken > fish>dairy prod

220 enous leukemia (CML), but the persistence of CML stem cells hinders cure and necessitates indefinite

221 not TKIs, targets the stem cell potential of CML cells, including primary cells explanted from 12 CML

222 roliferation and colony-forming potential of CML stem and progenitor cells and reduced their growth i

223 from the BMM contributes to preservation of CML LSC following TKI treatment.

224 nd was associated with the poor prognosis of CML patients.

225 BCAT1 is upregulated during progression of CML and promotes BCAA production in leukaemia cells by a

226 derstanding of niche-dependent regulation of CML LSCs is required to eradicate disease.

227 eukemia (CML) is the intrinsic resistance of CML stem cells (CMLSCs) to the drug imatinib mesylate (I

228 ion, which was also present in a subclone of CML-SCs during the chronic phase in a patient who subseq

229 ncluding the identification of a subgroup of CML-SCs with a distinct molecular signature that selecti

230 upplemented diets, alleviate the symptoms of CML through their ability to activate the nuclear hormon

231 etion and signaling and enhance targeting of CML stem cells while sparing their normal counterparts.

232 d identification of novel target proteins of CMLs deserve special attention.

233 lymphocyte-associated antigen 4 (CTLA-4) on CML-LSCs but not normal hematopoietic stem cells and thi

234 and improves therapeutic efficacy of ATO on CML and xenograft tumor model.

235 fore, we recommend further investigations on CML-like BCR-ABL1-positive ALL.

236 al features, making them distinct from other CML or AML progenitor cells and from normal haematopoiet

237 o imatinib, which was approved for pediatric CML in 2003, the second-generation TKIs dasatinib and ni

238 es encountered in the treatment of pediatric CML (suboptimal response, poor treatment adherence, grow

239 phase, no progression toward advanced phase CML occurred, and all relapsing patients regained MMR an

240 the majority of patients with chronic phase CML achieving long-term disease control.

241 In vitro treatment of immature chronic phase CML cells with TKI alone, or in combination with interfe

242 CML cells from chronic phase CML patients as well as the blast crisis phase cell line

243 Ex vivo treated cells from chronic phase CML patients showed limited changes in TNT formation sim

244 when emerging in patients with chronic-phase CML across various TKIs.

245 Studies in patients with chronic-phase CML have shown that around 50% of patients who achieve a

246 nilotinib-naive patients with chronic-phase CML.

247 ase inhibitor therapy in early chronic-phase CML.

248 neated a panel of novel frequently presented CML-exclusive peptides.

249 , as a novel therapeutic approach to prevent CML relapse and, in combination with TKIs, enhance induc

250 enotransplanted with patient-derived primary CML cells.

251 viability and increased apoptosis in primary CML CD34(+) cells, with no effect on healthy CD34(+) cel

252 and class II-restricted peptides in primary CML samples.

253 R-ABL1 and reduced cell viability in primary CML stem cells.

254 presence of IL1RAP(+) cell lines or primary CML cells, resulting in secretion of proinflammatory cyt

255 tional assays, we demonstrate that primitive CML cells rely on upregulated oxidative metabolism for t

256 s and existence of an autocrine loop promote CML-primitive cells' TKI resistance.

257 Mechanistically, PTN promoted CML stem cell survival and TKI resistance via induction

258 tor-associated protein (IL1RAP) in quiescent CML stem cells may offer an opportunity for a permanent

259 PCs were found to significantly reduce CML (31.77%-87.56%), even at the lowest concentration, w

260 (+)-Catechin reduced CML levels the most, probably due to its structure-antio

261 tic cell-specific deletion of PTN suppressed CML development in BCR/ABL+ mice, suggesting that cell-a

262 f this PGE1-EP4 pathway specifically targets CML LSCs and that the combination of PGE1/misoprostol wi

263 Our results demonstrate that CML cells express low levels of TNTs, but CML therapeuti

264 We report that CML stem cells upregulate the expression of pleiotrophin

265 We recently showed that CML LSCs depend on Tcf1 and Lef1 factors for self-renewa

266 Strong evidence now shows that CML LSCs are resistant to the effects of TKIs and persis

267 ML and sRAGE were measured by ELISA, and the CML/sRAGE ratio was calculated.

268 , but these do not effectively eliminate the CML stem cells.

269 concentrations in older adults; however, the CML/sRAGE ratio remained similar across groups.

270 A8, uncovering a possible involvement of the CML protein family in the modulation of plant-autoinhibi

271 Additionally, cell surface expression of the CML stem cell markers CD25, CD26, and IL1RAP is high in

272 s expose a considerable heterogeneity of the CML stem cell population and propose a Lin(-)CD34(+)CD38

273 re were no significant associations with the CML/sRAGE ratio.

274 infant formula significantly contributes to CML levels.

275 kinase activity of BCR-ABL1 have transformed CML from a once-fatal disease to a manageable one for th

276 Treatment of transgenic CML mice in vivo with NIL in combination with WNT974 sig

277 model and a xenograft model of transplanted CML patient CD34(+) stem/progenitor cells.

278 BCL6, we demonstrated that in an IM-treated CML line the antiapoptotic effect of IFNgamma was indepe

279 poptotic effect of IFNgamma in an IM-treated CML line.

280 Unfortunately, CML and GIST have high rates of recurrence in the absenc

281 ated with free plasma MG-H1 and free urinary CML (beta = 0.23; 95% CI: 0.02, 0.43; and beta = 0.28; 9

282 IITA and MHC-II significantly increased when CML stem/progenitor cells were treated with the JAK1/2 i

283 the most substantial decline of deaths with CML, whereas AML deaths continued to rise in the past 20

284 CD34(-)) cells derived from individuals with CML, and we compared the signature of these cells with t

285 mission, and prolonged survival of mice with CML.

286 alysis of nonleukemic SCs from patients with CML also provided new insights into cell-extrinsic disru

287 er conditions afflicting them, patients with CML and comorbidities may aim for a near-normal life exp

288 linical development testing in patients with CML and Philadelphia chromosome-positive (Ph(+)) acute l

289 Results T cells of patients with CML at diagnosis expressed low l-selectin (CD62L) levels

290 immunologic configurations in patients with CML determine their response to therapy cessation and th

291 c effect, and applied it to 21 patients with CML for whom BCR-ABL1/ABL1 time courses had been quantif

292 oexistence of comorbidities in patients with CML not only may affect TKI selection but also demands c

293 nhibitor (TKI) imatinib allows patients with CML to experience near-normal life expectancy.

294 the favorable outcome of most patients with CML treated with tyrosine kinase inhibitors (TKIs), a gr

295 than 10 years of follow-up in patients with CML who were treated with imatinib as initial therapy.

296 tion with tigecycline to treat patients with CML with minimal residual disease.

297 spectively discontinued in 100 patients with CML with UMRD sustained for at least 2 years.

298 ficantly increased survival of patients with CML, and deep responders may consider stopping the treat

299 oved the clinical outcomes for patients with CML, with over 80% of patients treated with imatinib sur

300 treated and imatinib-resistant patients with CML.